Mycobacterium tuberculosis

Mycobacterium tuberculosis

Organism

Mycobacterium tuberculosis is an acid-fast, rod-shaped bacterium approximately 0.4µm by 3.0µm. Acid-fast refers to the fact that because of its unique cell wall, when stained by the acid-fast procedure it will resist decolorization with acid-alcohol and stain red, the color of the initial stain, carbol fuchsin. With the exception of a very few other acid-fast bacteria such as Nocardia, all other bacteria will be decolorized and stain blue, the color of the methylene blue counterstain.
It is an obligate aerobe (def).
Because of its fastidious (def) nature and a relatively impermeable cell wall, M. tuberculosis is slow growing, dividing only every 12-24 hours.
The cell wall also renders it resistant to many disinfectants and antibiotics.

Habitat

Found in infected humans.

Source

Inhalation of aerosolized (def) infectious particles from close person-to-person contact.

Epidemiology

An estimated one-third of the world's population, approximately 1.9 billion people, are thought to be infected with M. tuberculosis.
It is estimated by the World Health Organization that worldwide, there are over 8,800,000 million new cases of tuberculosis each year and nearly 3,000,000 deaths.
The disease is most prevalent in sub-Saharan Africa, Southeast Asia, and Eastern Europe.
There are approximately 20,000 newcases of tuberculosis a year in the U.S.
In the U.S. tuberculosis is most prevalent in immigrants, drug or alcohol abusers, the homeless, and immunocompromised individuals.

Clinical Disease

Usually restricted to the lungs in immunocompetent patients but may spread by way of the blood to any organ in immunosuppressed patients.
Around 5% of people exposed to M. tuberculosis progress to having active disease within 2 years; an additional 5%-10% develop disease sometime later in life.
Progression from exposure to M. tuberculosis and progression to active pulmonary disease is a function of the number of bacteria entering the body and the competence of the person's immune system.
Effectiveness of elimination of the bacteria is partly related to the size of the focus of infection.
Typical symptoms are malaise (def), weight loss, cough, and night sweats. Sputum can range from scant to bloody and purulent (def).

Pathogenicity

When M. tuberculosis enters the lungs it penetrates unactivated alveolar macrophages (def) and and inhibits the acidification of phagosomes (def) needed for lysosomal enzymes to kill the bacteria. M. tuberculosis replicates freely in these alveolar macrophages eventually destroying them and spreading to other cells.
Most disease symptoms and damage to the body is a result of immune responses to the bacterium. Eventually activated macrophages (def) engulf and kill the bacteria while cytotoxic T-lymphocytes (def) kill M. tuberculosis-infected cells. If the bacterial load is small at this time the bacteria are destroyed with minimal tissue damage. However, if the bacterial load is high, production of inflammatory cytokines, activation of the complement pathways, and the hydrolytic enzymes and toxic oxygen radicals produced by macrophages lead to considerable tissue death.
If the intial foci of infection are small and the localized accumulations of activated macrophages (called granuloma (def)) are less than 3 millimeters, the activated macrophages usually contain and kill the M. tuberculosis. However, when larger granuloma develop in areas with more tissue necrosis (def), they become encased in fibrin (def) and the bacteria are protected from macrophage killing. In this state the M. tuberculosis can remain dormant for years and be reactivated if immune defenses weaken as a result of aging, immunosuppressive diseases, or immunosuppressive treatments. The formation of granuloma is actually the result of cell-mediated immune responses attempting to wall-off and localize infections that the body cannot effectively remove with macrophages.

Treatment

Common drugs used to treat and prevent tuberculosis include isoniazid, rifampin, pyrazinamide, ethambutol, levofloxacin, and streptomycin. (see antibiotic table)
CDC treatment recommendations

For a more detailed article on tuberculosis, see Tuberculosis, by Thomas Herchline, MD, Associate Professor, Department of Internal Medicine, Division of Infectious Disease, Wright State University and Judith K Amorosa, MD, FACR, Clinical Professor and Program Director, Department of Radiology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School; Consulting Staff, Department of Radiology, Robert Wood Johnson University Hospital